Radiolucent Lesions of Jaw

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PICTORIAL REVIEW

Radiolucent lesions of the mandible: a pattern-based

approach to diagnosis

Laurène Avril & Tommaso Lombardi & Angeliki Ailianou &

Karim Burkhardt & Arthur Varoquaux & Paolo Scolozzi &

Minerva Becker

Received: 20 September 2013 / Revised: 1 November 2013 /Accepted: 6 November 2013 / Published online: 10 December 2013# The Author(s) 2013. This article is published with open access at Springerlink.com

Abstract

Objectives Radiolucent mandibular lesions seen on panoram-

ic radiographs develop from both odontogenic and non-odontogenic structures. They represent a broad spectrum of

lesions with a varying degree of malignant potential. The

purpose of this review is to illustrate the characteristic imaging

findings — as well as the clinical and histological features — of

common and uncommon radiolucent lesions of the mandible.

Methods This review article is based on the retrospective

evaluation of 11,725 panoramic radiographs seen in our insti-

tution during the past 6 years. It provides a comprehensive,

practical approach to the radiological interpretation of radio-

lucent lesions of the mandible. To facilitate the diagnostic

approach, we have classified radiolucent lesions into two

groups: lesions with well-defined borders and those with ill-

defined borders.

Results Lesion prevalence, age of manifestation, location

within the mandible, relationship to dental structures, effect

on adjacent structures and characteristic findings at computed

tomography (CT), cone beam CT (CBCT) and magnetic

resonance imaging (MRI) with diffusion-weighted imaging

(DWI) are discussed. Pitfalls including malignant lesions

mimicking benign disease and pseudo-lesions are equally

addressed.Conclusion Knowledge of the characteristic imaging features

of radiolucent mandibular lesions narrows the differential

diagnosis and is crucial for the identification of those lesions,

where biopsy is indicated for definitive histology.

Teaching points

• Panoramic X-rays, CT and MRI are essential for the work-

up of radiolucent mandibular lesions.

• Lesion borders, location within the mandible, relationship to

dental structures and tissue characteristics on cross-

sectional imaging are indispensable to narrow the differen-

tial diagnosis.

• High-resolution CT and CBCT play a major role for the

assessment of lesion margins and their relationship to im-

portant anatomic structures, such as the inferior alveolar

nerve.

• Although most radiolucent lesions with well-defined sclerot-

ic borders are benign, MRI may reveal clinically unsuspect-

ed malignant disease.

Keywords Mandible . Radiolucent lesions . Panoramic

radiography . Computed tomography (CT) . Magnetic

resonance imaging (MRI)

Abbreviations

ADC Apparent diffusion coefficient

AAOMS American Association of Oral and Maxillofacial

Surgeons

BRONJ Bisphosphonate-related osteonecrosis of the jaw

CBCT Cone beam computed tomography

CT Computed tomography

DWI Diffusion-weighted imaging

EG Eospinophilic granuloma

GCG Giant cell granuloma

L. Avril : A. Ailianou : A. Varoquaux : M. Becker (*)

Department of Radiology, University Hospital of Geneva,

University of Geneva, Rue Gabrielle-Perret-Gentil 4,1211 Geneva 14, Switzerland

e-mail: [email protected]

T. Lombardi : P. Scolozzi

Department of Maxillo-Facial Surgery, University Hospital of

Geneva, University of Geneva, Rue Gabrielle-Perret-Gentil 4,

1211 Geneva 14, Switzerland

K. Burkhardt

Department of Clinical Pathology, University Hospital of Geneva,

University of Geneva, Rue Gabrielle-Perret-Gentil 4,

1211 Geneva 14, Switzerland

Insights Imaging (2014) 5:85 – 101

DOI 10.1007/s13244-013-0298-9


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HL Hodgkin lymphoma

KCOT Keratocystic odontogenic tumour

LCH Langerhans cell histiocytosis

MRI Magnetic resonance imaging

NHL Non-Hodgkin lymphoma

OPT Orthopantomography

ORN Osteoradionecrosis

PET/CT Positron emission tomography combinedwith CT

PET/MRI Positron emission tomography combined

with MRI

SBC Simple bone cyst

SCC Squamous cell carcinoma

SUV Standardised uptake value

Introduction

Conventional radiography may reveal a variety of radiolucent

lesions in the mandible. These represent a broad spectrum of odontogenic and non-odontogenic lesions with a varying de-

gree of malignant potential. Interpretation of radiolucent le-

sions of the mandible can be challenging either because the

clinical presentation may be non-specific or because the lesion

may be detected incidentally [1, 2]. In some cases, the diag-

nosis will be mainly made based on clinical symptoms. In

other cases, although a thorough clinical evaluation is manda-

tory, clinical findings are non-contributory, as the lesion can-

not be seen or palpated and laboratory findings are not abnor-

mal. Imaging is essential not only for the diagnosis of man-

dibular lesions but also to guide therapy and to monitor

treatment response. Although common, mandibular lesions

are not frequently imaged by radiologists. Nevertheless, their

recognition is essential for a rapid and correct diagnosis. This

review provides a comprehensive, practical approach to the

radiological interpretation of radiolucent lesions of the man-

dible and discusses their clinical presentation and pathophys-

iology. It focuses on the radiological techniques used and their

respective role for the assessment of these lesions.

Imaging modalities

Due to the easy access and low radiation dose, conventional

r ad io gr ap hs s uc h a s p an or am ic r ad io gr ap hs

(orthopantomographies [OPTs] or panoramix X-rays) as well

as dental intraoral radiographs traditionally form the backbone

in the diagnosis of osseous changes in the mandible [1, 3]. In

addition, the introduction of digital radiographs has lead to

further dose reduction (up to 80 %) with the possibility of

densitometric and subtraction techniques [4]. Conventional

radiographs of the mandible, typically OPTs, may reveal

radiolucent, radiodense or mixed pattern lesions [1, 3]. In

many cases, such as in radicular cysts, the diagnosis is

straightforward and no additional imaging is required for

diagnosis and treatment. As conventional radiographs are

two-dimensional projections of three-dimensional structures,

they have a limited value for the assessment of lesion size, lesion

margins, as well as extension into important anatomic structures

or soft tissues. Computed tomography (CT), cone beam CT

(CBCT), magnetic resonance imaging (MRI) and positron emis-sion tomography combined with CT (PET/CT) and more re-

cently positron emission tomography combined with MRI

(PET/MRI) complement conventional radiographs overcoming

the above-mentioned limitations and providing more specific

information in terms of diagnosis and therapeutic options.

Thin-slice (1-mm), high-resolution CT with bone window

settings is mainly used pre-operatively to precisely assess

lesion size, margins, destruction and expansion patterns, as

well as the relationship of the lesion to the mandibular canal.

Although coronal slices are sufficient in many situations,

dental CT with orthoradial and panoramic reconstructions

are superior to standard coronal reconstructions for the eval-uation of the relationship of a lesion to the dental structures

and to the mandibular canal. Intravenous contrast material is

mainly used in cases of suspected jaw infection or in neoplas-

tic diseases to assess the intraosseous and extraosseous in-

volvement. Although CBCT has gained increasing popularity

over the past years, it does not allow evaluation of

extraosseous structures; use of CBCT may therefore lead to

underestimation of disease extent.

High-resolution MRI is mainly used as a complementary

tool to CT or CBCT, as it allows precise depiction of

intraosseous and extraosseous lesion components, cyst wall

architecture (thin versus irregular walls, mural nodules, pap-

illary projections), enhancement patterns after intravenous

administration of gadolinium chelates (mild to strong), and

type of soft tissue involvement (displacement versus infiltra-

tion) [5]. In inflammatory and infectious lesions, MRI is more

sensitive than CT or CBCT for the detection of bone marrow

involvement [6].

Diffusion weighted imaging (DWI) is a functional MRI

technique based on the assessment of random (Brownian)

motion of water molecules. Biological barriers can impair

the free displacement of water molecules, thus resulting in

restricted diffusivity. Restricted diffusivity is seen in a variety

of conditions, including stroke, tumours with increased cellu-

larity, infection and inflammation, as well as abscesses.

Diffusion in biological tissues can be quantified using the

apparent diffusion coefficient (ADC). ADC measurements

(in mm2/s) have been shown to be reproducible with excellent

intraobserver and interobserver reproducibility in the head and

neck [7]. MRI with DWI and ADC measurements helps in the

differential diagnosis of cysts, ameloblastomas and malignant

tumours (see below). Although ADC values cannot predict the

histological grade in head and neck squamous cell carcinoma

86 Insights Imaging (2014) 5:85 – 101


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(SCC), lower values are observed in poorly differentiated

lesions whereas higher values are seen in well-differentiated

tumours [7]. In lymphomas, ADC measurements typically

yield very low values (see below).

As a general rule, PET/CT is uncommonly used for the

work-up of mandibular lesions. Nevertheless, it may be

employed as a complementary examination for the staging

of malignant tumours invading the mandible, such as SCC of the oral cavity with secondary mandibular invasion, in prima-

ry intraosseous SCC or in mandibular lymphoma. In cases of

metastases to the mandible, PET/CT may reveal the location

of the primary tumour — if unknown — or may effectively

show involvement of multiple organs. The most commonly

used radiotracer is 18F-fluorodeoxyglucose (FDG). FDG is a

glucose analogue that is taken up by metabolically active

tumour cells using facilitated glucose transport. In clinical

routine, quantification of tracer uptake is performed using

the standardised uptake value (SUV). High SUVs reflect high

glucose metabolism mainly seen in aggressive tumours (typ-

ically SCC and lymphoma), while lower SUV values arerather seen in slowly growing, less aggressive tumours, in

tumours with large areas of necrosis or in inflammatory con-

ditions. The recent implementation of integrated hybrid PET/

MRI systems in clinical head and neck oncology [8] holds

promise as it combines morphological, functional and molec-

ular information at the same time, thereby providing addition-

al diagnostic gain. However, research into the potential clin-

ical role of PET/MRI in comparison with PET/CT, MRI with

DWI or the combination thereof, is still ongoing.

This review article is based on the retrospective evaluation of

11,725 panoramic radiographs seen during a period of 6 years at

our institution. From a practical point of view, radiolucent

mandibular lesions can be divided into lesions with well-

defined borders and lesions with poorly defined borders.

Radiolucent lesions with well-defined borders

Radicular cyst

Odontogenic cysts are true cysts arising from the epithelium

left over from tooth development. Radicular cysts, also called

periapical cysts or apical periodontal cysts, are the most com-

mon odontogenic cysts [1, 2]. Tooth infection may lead to

necrosis of the pulp cavity and may spread to the tooth apex

with ulterior development of a periapical granuloma or

periapical abscess. The latter may subsequently give rise to a

radicular cyst. Radicular cysts arise from epithelial cell rests of

the periodontal ligament, which are stimulated by the inflam-

matory products. Most often, radicular cysts are asymptomat-

ic. They may be seen in all age groups, however, more often

between 30 and 60 years of age and are typically associated

with a non-vital tooth. Imaging features are straightforward

and include a unilocular periapical lesion with well-defined,

sclerotic borders in close vicinity of the apical portion of the

root of a non-vital tooth. No contrast material enhancement is

seen on CT or MRI. In atypical cases with latero-dental

location, CTor CBCT is very helpful for the correct diagnosis

(Fig. 1). Treatment options include apical surgery, tooth ex-

traction and endodontic treatment.

Residual cyst

Residual cysts are periapical cysts retained in the jaw after

surgical removal of a non-vital tooth [1, 3]. Residual cysts are

common and have similar clinical and radiological features as

radicular cysts. However, there is always a missing tooth

(Fig. 2). Most residual cysts are less than 1 cm in size.

Occasionally, enlarging cysts may cause displacement of the

adjacent teeth, as well as bone expansion.

Dentigerous cyst

Follicular cysts, also called dentigerous cysts or pericoronal

cysts, are the second most common odontogenic mandibular

cysts and the most common developmental cysts of

odontogenic origin. They are typically seen in patients aged

20 – 40. Once fluid accumulates between the enamel organ

Fig. 1 Radicular cyst. a OPT. Unilocular radiolucent lesion with well-

defined borders (asterisk ) displacing teeth 33 and 34. b CT, sagittal

oblique 2D MPR with bone windows. Cystic lesion surrounding the root

(dashed arrow) of the non-vital tooth 34. Associated large caries with

pulpal necrosis (arrow). c Histology (haematoxylin-eosin stain, original

magnification 20×): fibrous connective wall containing a dense chronic

inflammatory infiltrate and congested vessels (asterisk ) lined by irregular

non-keratinised stratified squamous epithelium. Spongiotic epithelium

(arrows) penetrated by neutrophils

Insights Imaging (2014) 5:85 – 101 87


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remnants and the tooth crown, a cyst forms around the crown

of the unerupted tooth (typically the lower third molar).

Imaging features of follicular cysts are characteristic and

include a unilocular, well-defined radiolucent lesion with

sclerotic borders around an unerupted tooth crown (Fig. 3).

Small follicular cysts may be difficult to differentiate from a

normal dental follicle. It has been suggested that when the

distance between the crown and the dental sac is superior to3 mm, the diagnosis of a follicular cyst should be made. The

cyst is most often attached to the neck of the unerupted and

displaced tooth, and the crown generally protrudes into the

cyst while the roots remain outside the lesion (Fig. 3).

Follicular cysts may become very large [9] and may remodel

the mandible, predisposing the patient to pathological fracture

and infection. They may thin the cortical layer of the mandible

and may insinuate around the mandibular canal, making sur-

gical excision risky. CT and CBCT are used to determine the

relationship of the cyst to the mandibular canal prior to sur-

gery and to assess cyst contents, as well as integrity of the

cortical rim (Fig. 3). MRI is indicated only in atypical cases to

differentiate follicular cysts from other cystic mandibular le-

sions [5]. Follicular cysts will often be found incidentally in

patients undergoing head and neck MRI for other indications.

MRI findings include variable signal intensity on T1 due to

variable protein content within the cyst, high signal on T2 and

occasionally slight enhancement of the thin cyst wall.

Although most cysts show no significant FDG uptake on

PET/CT, mild tracer uptake may be seen in the presence of

infection or inflammation [10]. Treatment options include

enucleation in smaller lesions and marsupialisation in larger

cysts. Rarely, SCC ( see “Pitfalls”) or ameloblastoma may

arise from the epithelium of the cyst wall [11 – 13]. Multiple

follicular cysts are very rare and may be seen in cleidocranial

dysplasia, muccopolysaccharidosis type 4 [9] and in the

Gorlin-Goltz syndrome.

Keratocyst

Keratocysts, also called primordial cysts, keratinising cysts or

keratocystic odontogenic tumours (KCOTs), are benign

intraosseous tumours arising from the dental lamina [11].

They are lined by stratified keratinising epithelium. Due to

their potentially aggressive, infiltrative behaviour, they have a

high recurrence rate after surgery (up to 60 %) [1, 14, 15].

KCOTs are often asymptomatic. They are often misdiagnosed

as periapical cysts, follicular cysts, lateral periodontal cysts or

ameloblastoma [14]. According to the literature, KCOT have

a periapical position in 33 % of cases, a pericoronal position in

21 % of cases, a lateral root position in 19 % of cases and arenot related to any dental structures in 27 % of cases [ 14].

KCOTs essentially occur in the 2nd and 3rd decade in the

posterior body or in the ascending ramus of the mandible.

Lesions in the molar and premolar area or in the anterior

mandible are less common. Men are affected more commonly

than women, most KCOTs occurring in Caucasian popula-

tions of Northern European decent. As KCOTs may become

very large, they tend to remodel, hollow and expand the

mandible (Fig. 4). Smaller lesions tend to be unilocular, while

larger lesions tend to be multilocular. KCOTs show well-

delineated, sclerotic or scalloped borders, soft-tissue extension

and daughter cysts. The adjacent teeth are only rarely re-

sorbed; however, when this is the case, differentiation from

ameloblastoma may be very difficult on OPT, CT or CBCT.

As KCOTs contain a cheese-like material, they typically show

soft tissue density (up to 50 HU) on CT (Fig. 4), while on

MRI, due to the variable protein content, a low to high signal

intensity may be seen on T1 and a heterogeneous signal on T2.

T2 relaxation times in KCOT have been reported to be shorter

than in ameloblastoma [5]. Weak enhancement of the uni-

formly thin and regular cyst walls is noted after injection of

gadolinium chelates, thereby facilitating differentiation from

ameloblastoma [5].

Multiple KCOTs are seen in the nevoid basal cell carcinoma

syndrome (Gorlin-Goltz syndrome), the oral-facial-digital syn-

drome, the Ehlers Danlos and in the Noonan syndrome [2, 16].

The Gorlin-Golz syndrome is an autosomal dominant disorder

manifesting with mental retardation, multiple KCOTs (Fig. 5),

basocellular carcinomas, bone defects, subcutaneous and falx

cerebri calcifications. Patients typically have large calvaria,

midface hypoplasia, high-arched eyebrows and hypertelorism.

The treatment of choice in KCOTs is complete surgical re-

moval of the lesion itself, including the commonly associated

Fig. 2 Residual cyst. a OPT.

Unilocular well-defined lesion

with sclerotic borders (arrow)

and missing tooth 36 above. b

Histology (haematoxylin-eosin

stain, original magnification 20×):

non-keratinised stratified

squamous epithelium (arrow)

with mild inflammation



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tooth. Careful clinical and radiological post-operative follow-

up is essential due to the high recurrence rate.

Ameloblastoma

Ameloblastomas are benign but locally invasive, slowly

growing odontogenic tumours arising from remnants of the

dental lamina and dental organ or, less frequently, from the

epithelial lining of an odontogenic cyst [12]. They represent

10 % of all odontogenic tumours, most lesions being located

in the mandible (posterior body and ramus region). Most

tumours tend to occur during the 4th – 6th decade and there is

no sex predilection. Clinical features are non-specific and

patients may complain of unilateral painless swelling. Very

often, ameloblastomas are detected incidentally. Although

classic amelobastomas do not have distant metastases, vari-

ants with metastatic behaviour despite histologically benign

features (so-called “malignant ameloblastoma ”), as well as

tumours with histologically malignant features but without

metastatic potential (so-called “ameloblastic carcinomas”)

have been described in the literature [3]. Ameloblastomas

may be subdivided into four histological types: unicystic,

multicystic, extraosseous, and desmoplastic [12]. The radio-

logical appearance depends on the histological type and

Fig. 3 Dentigerous cyst. a OPT, b axial CT with bone windows and c

dentascan reconstruction. Unilocular well-defined radiolucent lesion

(thick arrows) surrounding an unerupted tooth. Immediate vicinity of

the mandibular canal (dashed arrow) to the impacted tooth. d Three-

dimensional reconstruction, lateral view showing the relationship of the

cyst (blue), the unerupted tooth ( green) and the mandibular canal (red ).

The cyst is attachedat thelevel of thetoothneck andsurrounds thecrown.

e Surgical specimen. Characteristic attachment of the cyst at the tooth

neck (arrows). f Histology (haematoxylin-eosin stain, original magnifi-

cation 20×): non keratinising thin epithelial lining (arrow) without rete

pegs. Fibrous wall (asterisks ) almost completely devoid of inflammatory

cells

Fig. 4 Histologically proven KCOT. a OPT. Axial CT image with bone

window (b) and soft tissue window (c). Multilocular well-defined radio-

lucent lesion (asterisk ) with thin, sclerotic borders, cortical scalloping

(arrow) and resorption of teeth roots. Cyst contents with attenuation

values of 40 – 50 HU mimicking solid tissue. d Posterior view of a 3D

reconstruction showing the relationship between the keratocyst (blue),

the partially resorbed teeth ( green) and the mandibular canal (red ). The

mandibular canal can be seen only in the posterior mandible, as it is

encased by the keratocyst



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includes unilocular or multilocular radiolucent lesions (“soap

bubble” or “honeycomb” appearance) with sclerotic borders,

displaced adjacent teeth with root resorption and/or extensive

bone expansion (Figs. 6 and 7). CTand MRI are used toassess

tumour contents, integrity of the mandibular cortical rim,

relationship to the mandibular canal and precise intraosseous

and soft tissue extension (Figs. 6 and 7). In multicystic

ameloblastoma, MRI reveals cysts with variable protein con-

tent. Typically, after injection of gadolinium chelates, MRI

shows enhancement of solid nodular components, of irregu-

larly thick septations and of papillary projections (Fig. 6).

Although differentiation between benign and malignant

ameloblastoma may be impossible with CT and MRI, a very

high FDG uptake on PET/CT strongly suggests malignant

ameloblastoma or ameloblastic carcinoma [17]. Treatment

consists in complete surgical excision and careful post-

operative follow-up with imaging is mandatory.

Simple bone cyst

The simple bone cyst (SBC), also known as solitary bone cyst,

traumatic bone cyst, haemorrhagic cyst or idiopathic bone

cavity is filled with serous or haemorrhagic fluid and is

characterised by the absence of an epithelial lining.

Therefore, SBC is not a true cyst but rather a pseudocyst.

SBC of the mandible usually occurs secondary to trauma,

typically after tooth extraction with subsequent intramedullary

haemorrhage. Most SBCs occur before the age of 20 with

female predominance [18]. In up to 75 % of all cases, SBCs

are seen in the marrow of the posterior mandible. Most lesions

are asymptomatic and discovered incidentally on dental

radiographs. SBC occurs in close proximity to a vital tooth

and is not associated with bone swelling unless there is

Fig. 5 Basal cell nevus

syndrome. a OPG. Multiple

mandibular and maxillary KCOTs

(asterisks ) associated with

impacted teeth. b Intraoperative

view showing cheese-like

material within the angulo-

mandibular lesion (arrow). c

Surgical specimen showing the

KCOT (asterisk ) and theassociated tooth (thin long

arrow). d Histology

(haematoxylin-eosin stain,

original magnification 40×):

corrugated (dashed arrows)

parakeratinised epithelium with

distinct basal columnar cells with

inverted polarity (arrows) and flat

connective tissue interface

Fig. 6 Histologically proven multilocular ameloblastoma. a Axial bone

window CT image. b Three-dimensional reconstruction, frontal view. c

T1-weighted axial image. d T1-weighted axial image after injection of

gadolinium chelates. Multilocular expansile radiolucency with character-

istic “soap bubble” appearance (asterisks ) and major facial deformation.

Cystic components with variable signal intensity on the unenhnanced T1-

weighted image suggesting variable protein content. Note variable en-

hancement of solid components ranging from thin enhancing walls to

thick enhancing solid portions (arrows)



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associated infection. Surgical exploration may be necessary in

selected cases to exclude other unilocular radiolucent lesions,

such as keratocysts. On imaging, most SBCs appear as uni-

locular, well-defined radiolucent lesions that vary in size.

Rarely, poorly defined borders are observed. Extension to

the cortical bone is rare and usually there is no tooth displace-

ment [18]. The superior margins are irregular and scallop

around teeth roots. CT and MRI can provide information on

the haemorrhagic content but the density or signal intensity,

respectively, may vary depending on the age of the haemor-

rhage. On MRI, the cysts display a homogeneous intermediate

signal on T1, homogeneous high signal on T2, and no en-

hancement after injection of intravenous contrast media.

Treatment consists of bone curettage, leading to bleeding with

subsequent scar formation.

Eosinophilic granuloma of the mandible

Eosinophilic granuloma (EG) is a benign disease related to

any of the three forms of Langerhans cell histiocytosis (LCH).

Depending upon the number of lesions and lesion distribution,

LCH comprises the following groups: unifocal LCH (also

called EG), multifocal unisystem and multifocal multisystem.

The combination of diabetes insipidus, lytic bone lesions and

exophtalmus is known as Hand-Schüller-Christian triad,

whereas the multifocal multisystem LCH is also called Abt-

Letterer-Siwe disease (with typical abdominal involvement

and poor prognosis) [19]. LCH is caused by clonal prolifera-

tion of activated dendritic cells and macrophages [20]. Any

bone can be affected, such as the skull, mandible, ribs and

long bones, as well as any organ system (lung, skin, spleen,

lymph nodes, central nervous system). Therefore, cross-

sectional whole-body imaging is essential for the initial

work-up of patients with active disease and for post-

therapeutic follow-up purposes.

The incidence of mandibular EG constitutes less than 10 %

of all LCH cases. LCH often affects males in the 1st – 3rd

decade, although most cases are seen in children younger than

15 years of age. Mandibular involvement is seen preferentially

in the body or angle (Fig. 8). Clinical presentation can be

silent or non-specific including pain, swelling, fever, general

malaise, gingival hypertrophy, ulcers of the buccal mucosa,

limitation of mouth opening or tooth hypermobility and loos-

ening. Pathological fracture may ensue. Radiologically, EG

presents as a well-defined radiolucent lesion, with or without

reactive sclerosis on OPT; however, an accompanying perios-

teal reaction is typically seen on CT or CBCT. Occasionally,

this periosteal reaction may show a sunburst appearance,

suggesting a more aggressive biological behaviour. If the

alveolar crest is invaded, a “scooped out ” appearance is seen;

when the alveolar bone is destroyed, a “floating tooth” ap-

pearance is observed. EG is often associated with a soft tissue

mass surrounding the mandible and invading the muscles of

mastication. Morphological MRI findings include hypointense

signal on T1, hyperintense signal on T2 and marked enhance-

ment after intravenous gadolinium (Fig. 8). In our experience,

ADC values in EG are usually slightly higher than in malignant

lesions (≥1.2×10−3 mm2/s versus±1×10−3 mm2/s). In cases

Fig. 7 Recurrent multilocular

ameloblastoma. a OPT showing a

well-defined, multilocular

radiolucency (arrows) with

sclerotic borders. b Resected

specimen and c specimen

radiograph clearly show bony

expansion, destruction of the

alveolar ridge and characteristic

multilocular appearance. dHistology (haematoxylin-eosin


follicular ameloblastoma with

squamous metaplasia (red

asterisks ) within follicles

(arrows). Largely fibrous stroma

(black asterisks) containing

scattered lymphocytes



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with atypical periosteal reaction and poorly defined margins,

the differential diagnosis includes malignant tumours, such as

osteosarcoma, Ewing sarcoma or metastases. Nevertheless,

well-defined margins on CT, the high signal intensity on T2,

the strong enhancement, the large area of inflammatory oedema

and the moderately high ADC values rather suggest a lesion

with benign histology (Fig. 8). The value of MRI in patients

with EG lies in its high sensitivity especially when used in

conjunction with DWI [20]. PET/CT has been shown to pro-

vide valuable information for the detection of EG lesions due to

their high FDG uptake (Fig. 8) and it has been suggested that

hybrid PET/MRI may play a pivotal role for the primary

investigation of paediatric histiocytosis allowing accurate de-

tection of multifocal multiorgan involvement and for monitor-

ing treatment response [20]. Despite the relatively charac-

teristic imaging findings, definitive diagnosis of EG is

made on samples obtained by biopsy. Treatment modalities

include surgery, chemotherapy and intralesional injection

of corticosteroids.

Giant cell granuloma

Giant cell granuloma (GCG) is a benign but occasionally

aggressive proliferative intraosseous lesion with fibrous tis-

sue, haemorrhage and haemosiderin deposits, as well as

characteristic osteoclast-like giant cells. GCG is a rare lesion

occurring preferentially in young girls or women [1, 21]. The

posterior mandible is affected more often than the anterior

mandible. Multifocal involvement is seen in hyperparathy-

roidism, cherubism or Noonan syndrome [21, 22]. The most

common clinical features are pain, swelling, facial asymmetry

and paresthesia. Differential diagnosis includes giant cell tu-

mour, radicular cyst, ameloblastoma, odontogenic tumour and

fibrous dysplasia. The typical radiological appearance is that

of a multilocular (less often unilocular) well-defined radiolu-

cent lesion. However, ill-defined lesions have also been re-

ported. In some cases, bone may be expanded or teeth can be

displaced or resorbed. CT, CBCT and MRI are useful for

describing bony involvement and for evaluating extension

into the adjacent soft tissues. On MRI, GCG has a homoge-

neous or slightly heterogeneous intermediate signal on T1, T2

and STIR (short TI inversion recovery) and shows moderate

to strong contrast enhancement after administration of gado-

linium. However, it is important to note that only very few

data regarding the imaging characteristics of GCG are cur-

rently available in the literature. The treatment of choice is

surgery (enucleation and curettage in well-defined GCG or en

bloc resection in aggressive GCG) and medical treatment

(intralesional corticosteroid or calcitonin injections) [21].

Recurrence may occur in up to 15 % of cases.

Fig. 8 Histologically proven eosinophilic granuloma. a OPT-like curved

thick slab reconstruction, b axial CT bone window and (c) 3D recon-

struction from CT data set show a well-defined radiolucent lesion (ar-

rows ) located in the angle of the mandible. Sharply delineated slightly

sclerotic borders. Periosteal reaction (dashed arrow). d PET/CTshowing

that high FDG uptake within the posterior mandible and perimandibular

soft tissues (arrow). SUVmean = 6, SUVmax = 9. e Axial T2 and f

sagittal T1 after intravenous gadolinium show a large extraosseous com-

ponent (arrows) with invasion of the masseter muscle. Close vicinity to

the submandibulat gland. Note high signal intensity on T2 and strong

enhancement after gadolinium. g Fused T2 and b 1,000 showing restrict-

ed diffusion. h ADC map showing a moderately low ADC value (ADC =

1.21×10−3 mm2/s, arrow) within the lesion. Note inflammatory oedema

around the lesion with high ADC values ( asterisk )



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Radiolucent lesions with ill-defined borders

Osteomyelitis

Despite the introduction of antibiotics and improved medical

care, osteomyelitis of the jaws is still relatively common. The

mandible is affected more often than the maxilla. Depending

on the clinical course, osteomyelitis of the mandible can beclassified into three forms: acute, secondary chronic and pri-

mary chronic [23, 24]. The acute and secondary chronic forms

are manifestations of the same disease entity separated by the

arbitrary time limit of 1 month. These two forms are typically

caused by bacterial infection in the setting of pulpal or peri-

odontal infection, mandibular foreign bodies, sepsis or trau-

ma. In dental infection, pulpal infection extends into the bone

marrow and there is compression of blood vessels from

periapical lesions. Acute forms present with severe symptoms

such as pain, swelling, fever, lymphadenopathy or a mobile

tooth sensitive to percussion. They may also present with

paresthesia in the lower lip (V3 nerve), trismus or fistula with pus and — in advanced stages — osteomyelitis may also be

revealed by pathological fractures. The chronic forms are

clinically silent but often include painful periods.

Predisposing factors are diabetes, immunosuppression, radio-

therapy and bisphosphonates.

While the diagnosis of osteomyelitis can be made clinically

in many cases, imaging is especially helpful to define the

extent and assess the severity of the lesion. The radiological

appearance of osteomyelitis depends on the stage of disease. It

consists of an ill-defined osteolytic lesion (Fig. 9), with bone

sequestra, and — in subacute cases — is often associated scle-

rosis and periosteal new bone formation. CT is helpful to

analyse the bone structure, to search for associated abscessesand to identify soft tissue extension (myositis, fasciitis, cellu-

litis). MRI findings in osteomyelitis are similar to those in

osteoradionecrosis (Fig. 9) and the differentiation between the

two entities is based on the clinical context. MRI is more

sensitive than CT in detecting marrow and soft tissue involve-

ment [25]. In addition, MRI allows earlier diagnosis of oste-

omyelitis than CT, CBCT or conventional radiographs. In

general, the disease extent appears larger on MRI than on

CT; therefore, a combined MRI and CT assessment is most

often required pre-operatively. Osteomyelitis lesions show

low signal on T1, and high signal on T2 and STIR images

due to oedema of the bony marrow; variable degrees of contrast enhancement of the marrow itself and of adjacent soft

tissues are equally observed (Fig. 9). The signal intensity of

bone sequestrae, however, is very low on all sequences.

Treatment consists of a combination of antibiotics and surgical

debridement.

Fig.9 Osteomyelitisafter tooth extraction. a OPT. b Contrast-enhanced,

axial CT image with bone window settings. c Three-dimensional recon-

struction. Ill-defined osteolytic area (asterisks ) extending into the ascend-

ing ramus of the mandible, with cortical destruction (arrows in b and c ).

d Axial T1-weighted image before (d) and after (e) injection of gadolin-

ium chelates. Hypointense signal of the mandible (arrows in d ) due to

marrow oedema and strong enhancement (arrows in e ) due to

hyperaemia. Myositis of the masseter muscle (thick dashed arrow) and

streaky enhancement of the subcutaneous fat and platysma muscle (thin

dashed arrow) suggesting a phlegmon. f Histology (haematoxylin-eosin

stain, original magnification 20×): non-viable trabeculae (large asterisks)

with bone resorption and destroyed osteoblasts. Inflammatory infiltrate

( small asterisks) with neutrophils and lymphocytes as well as increased

vascularisation within the fatty marrow



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Bisphosphonate osteonecrosis

Bisphosphonate treatment, similar to radiotherapy, may cause

bone necrosis. Bisphosphonates are widely used for the treat-

ment of cancer-related symptoms. Their benefits consist in

reducing hypercalcaemia, limiting progression of bone lesions

and preventing pathological fractures in bone metastases from

breast, prostate and lung cancer, as well as multiple myeloma [26]. In short, bisphosphonates are widely indicated to im-

prove the quality of life in a large number of patients.

Bisphosphonate-related osteonecrosis of the jaw (BRONJ)

was defined by the American Association of Oral and

Maxillofacial Surgeons (AAOMS) based on three criteria:

past or current bisphosphonate treatment, osteonecrosis last-

ing for at least 8 weeks and no history of radiotherapy to the

jaw. [26]. BRONJ most often occurs in the mandible rather

than the maxilla, especially in the molar region, and is fre-

quently triggered by a pre-existing focal lesion. Clinical fea-

tures include painful swelling, signs of infection (fever, oozing

pus, abscess and soft tissue inflammation) and a mobile toothsensitive to percussion. Occasionally, there is paresthesia in

the lower lip (whenever V3 is affected) or trismus. Imaging

features of BRONJ are the same as for osteoradionecrosis

(Fig. 10). MRI can show signal changes on T1 and T2 images

according to the stage of the disease. Although radiological

findings are easily identified, they are non-specific and the

final diagnosis is made by combining imaging findings with

the clinical context [27].

Osteoradionecrosis

Osteoradionecrosis (ORN) is a serious uncommon complica-

tion (2.6-15 %) of radiotherapy in head and neck cancer

patients. It usually occurs 5-15 years after radiotherapy. Therisk of developing ORN increases with poor oral hygiene,

alcohol and tobacco use after radiotherapy, tooth extraction

or periodontal disease prior to radiotherapy: ORN is also

related to the nutritional status of the patient. ORN preferen-

tially affects the molar, premolar and retromolar region.

Depending on the radiation portal and the administered radi-

ation dose, osteoradionecrosis may affect the mandible unilat-

erally or bilaterally. Combined treatment options (radiation

therapy, surgery and chemotherapy) appear to predispose to

ORN [28]. Clinical manifestations include pain, limitation of

mouth opening and deep ulcerations with denuded bone. In

advanced stages, trismus, fistulas and pathological fractureshave also been reported. CT usually reveals a patchy

radiopaque-radiolucent ill-defined lesion with cortical bone de-

struction, usually without periosteal reaction (Fig. 11). Typical

MRI findings are a mixture of marrow oedema (increased signal

on T2) and marrow sclerosis (reduced signal on T2) with

fragmentation of bone and sequestration (very low signal on

Fig. 10 Biphosphonate osteonecrosis. a OPT; b 3D reconstruction

anteo-lateral view. Contrast-enhanced axial CT image with bone window

settings (c ) and soft tissuesettings (d). Poorly defined osteolytic lesion of

the left mandibular body (thick white arrows) with partly sclerotic mar-

gins (thin arrows in a ) and large osseous defect (red arrows in b ). Bone

sequestra (dashed arrows). Associated subperiosteal phlegmon and myo-

sitis of the platysma (open arrows). e Histology (haematoxylin-eosin

stain, original magnification 20×): necrotic bone (large asterisk ) with

inflammatory infiltration of the fatty marrow ( small asterisks). Gingival

mucosa (arrows)



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12/17

diagnosis includes osteoid osteoma, ossifying fibroma,

periapical cemental dysplasia, fibrous dysplasia, as well as

other fibro-osseous lesions. Osteoid osteoma typically presents

with pain and a nidus can be identified at CT or CBCT.

Ossifying fibroma most commonly occurs in the posterior

mandible during the 3rd – 4th decades [1]. Depending on the

degree of calcification, the radiological appearance includes

well-defined radiolucent, radiopaque or mixed opacity lesions

[1]. Commonly, a radiolucent margin is seen on CT or CBCT,

allowing differentiation from fibrous dysplasia. Periapical

cemental dysplasia typically occurs in women during the 4th

and 5th decades. It is the consequence of connective tissue

proliferation within the periodontal membrane; therefore, the

lesions are typically located in vicinity of tooth apices [1].

Initially, the lesions are radiolucent and with increasing matu-

rity, there is advanced calcification. As opposed to mandibular

osteoblastoma and osteoid osteoma, many fibro-osseous lesions

do not cause pain despite their large size or associated teeth

displacement. In addition, the age of presentation, the multi-

plicity of lesions and the relationship to tooth apices are further

elements that help in the differential diagnosis. The treatment of

choice in osteoblastoma is surgery and recurrence is rare [31].

Some cases of spontaneous regression have been reported,

especially in young patients.

SCC with mandibular invasion

SCC, also known as epidermoid carcinoma, is a malignant

neoplasm arising from the mucosa of the oral cavity [32, 33].

It is the most common tumour of the oral cavity and prefer-

entially affects men over the age of 50. SCC most often occurs

in the mucosa overlying the posterior mandible, and it is

related to the consumption of alcohol and tobacco. It has high

metastatic potential. Clinical symptoms include pain, swell-

ing, paresthesia (due to V3 invasion) and dental disorders. In

advanced stages, SCC may be discovered in the context of a

pathological fracture. The radiological appearance is that of an

aggressive soft-tissue lesion with invasion of the floor of the

mouth, alveolar ridge or retromolar trigone [33]. In advanced

stages, secondary bone invasion can occur leading to the

appearance of an ill-defined radiolucent lesion of the mandible

on conventional X-rays; in advanced lesions, the “floating

teeth” sign may be equally observed due to extensive man-

dibular infiltration. On MRI, SCC displays a low to interme-

diate signal on T1, a moderately high signal on T2 and STIR

sequences, and a moderate enhancement after injection of

contrast media (Fig. 14). ADC values are typically low (usu-

ally around 1 – 1.1×10−3 mm2/s). Whenever large areas of

necrosis are present within the tumour, ADC values may,

however, be higher. This is particularly true in necrotic lymph

node metastases (Fig. 14). Lymph node metastases in SCC of

the oral cavity are common, especially in level I and II nodes.

On FDG PET/CTor PET/MRI, SUV values are typically high

due to the high glucose metabolism (Fig. 14). The final

diagnosis and the pre-therapeutic work-up in SCC of the oral

cavity are made by a combined clinical, imaging and histo-

logical work-up. The main role of imaging consists in precise-

ly depicting deep tumour spread, as well as detecting lymph

Fig. 13 Osteoblastoma. a OPT.

b Axial CT with bone window.

c Sagittal oblique contrast-

enhanced fat-saturated T1-

weighted image. Ill-defined

radiolucent lesion (arrows in a

and b ) with coarse sclerotic

borders and calcifications (dashed

arrow). Major contrast

enhancement (arrow in c ). dHistology (haematoxylin-eosin

stain, original magnification 64×).

Osteoid and woven bone

(asterisk ) with plump osteoblast-

like cells (arrows), interposed

fibroblasts and some

inflammatory cells



13/17

node and distant metastases. Surgery with or without radio-

therapy is the treatment of choice. Prognosis depends on the

histological type and on the presence or absence of lymph

node metastases.

Metastases

Metastases to the jaw are an uncommon entity, affecting the

mandible more often than the maxilla [34]. The most common

primaries vary depending upon gender. Lung, prostate, kidney

and liver tumours are the most common primaries in men,

whereas breast, adrenal, gynaecological and colorectal tu-

mours are the most common primaries in women [34].

Typical clinical symptoms include pain (Fig. 15), swelling,

paresthesia, temporomandibular joint derangement, but in

some cases metastases to the jaw are clinically silent and

found incidentally. The radiological appearance includes ill-

defined radiolucent lesions with no periosteal reaction on

conventional X-rays, CT and CBCT [35]. MRI reveals mod-

erately hyperintense masses on T2-weighted and STIR im-

ages, hypointense signal on T1-weighted images and variable

degrees of contrast enhancement. In general, the surrounding

soft tissues lack relevant oedema and enhancement unless

tumour extension beyond the mandible has occurred

(Fig. 15). On PET/CT, focal areas of increased FDG uptake

are typically observed and measured SUVs are high (Fig. 15).

Although the imaging aspect is not specific, in the presence of

a patient with a history of cancer, the diagnosis of mandibular

metastasis should be considered in the differential diagnosis

first, particularly when the lesion shows no relationship to

dental structures.

Pitfalls

Pseudolesions

Stafne cyst

Stafne cyst, also called static bone cavity or salivary gland

inclusion defect, is a pseudocyst arising from bone remodel-

ling caused by the adjacent submandibular gland. Therefore, it

does not present any epithelial lining. Stafne cysts are often

incidental findings, as patients are asymptomatic (Fig. 16).

The lesions are more common in men than in women. The

radiological aspect includes ovoid, well-defined radiolucent

cortical defects on the lingual surface of the posterior mandi-

ble usually measuring less than 2 cm. This location is typical

Fig. 14 SCC with mandibular invasion. Precise pre-operative assess-

ment with MRI and PET/CT. a OPT. Poorly defined bony destruction

(arrow) of the edentulous mandible. b Contrast-enhanced axial CT.

Aggressive soft-tissue lesion (arrow) with secondary bone invasion. c

Sagittal oblique PET/CT image. High metabolism of the tumour (black

asterisk , SUVmean = 18, SUVmax = 22) and of two metastatic level I

lymph nodes (arrows, SUVmean = 10, SUVmax = 15). d T2-weighted

axial image. Tumour (asterisk ) with marrow invasion and extensive

infiltration of the floor of the mouth (dashed arrow). Note two metastatic

level I lymph nodes (arrows). e The b 1,000 and f ADC map show

restricted diffusion within the tumour (circle, ADC = 0.98×10−3 mm2/s).

Variable ADC values within the metastatic lymph nodes due to the

presence of necrosis (arrows in f ). g Sagittal histological whole-organ

slice of the resected specimen. Tumour (dashed black line) invading the

mandible (black arrows) and the muscles (asterisk ) of the floor of the

mouth. The histological slice has the same orientation as (c )



14/17

and the lesion contains fat or salivary gland tissue. An OPT is

sufficient for diagnosis but occasionally CT or MRI can be

performed in cases of atypical presentation to exclude an

ameloblastoma or a traumatic bone cyst [2]. No treatment is

recommended; however, a follow-up examination at 3 –

6 months can be performed to ascertain lesion stability [3].

Malignant lesions mimicking benign disease

Intraosseous mucoepidermoid carcinoma

The vast majority of mucoepidermoid carcinomas arise within

the major or minor salivary glands. Primary intraosseous

mucoepidermoid carcinoma is an extremely rare tumour con-

stituting less than 2 % of all mucoepidermoid carcinomas. It

arises centrally within the angle or posterior mandible [36]. Its

aetiopathogenesis is not yet completely understood. Due to the

paucity of cases reported in the literature, little is known re-

garding age of presentation and sex distribution. Clinical fea-

tures include swelling and pain, as well as trismus. Imaging

features are unilocular or multilocular, well-defined lesions with

sclerotic borders, mimicking a benign cyst, a keratocyst or an

ameloblastoma on OPT, CT and CBCT [37]. On MRI, the

cystic tumour components display a low signal on T1, a high

signal on T2 and no enhancement, whereas the nodular solid

tumour components present a low signal on T2 and contrast

Fig. 15 Condylar metastasis

from adenocarcinoma. OPT (a)

with osteolytic ill-defined lesion

of the mandibular condyle

(arrow). b Sagittal PET/CT

image shows high metabolism

with SUV = 12 (arrow). c Axial,

contrast-enhanced, fat-saturated

T1-weighted image. The

infiltrative, bulky lesion invadesthe condyle (arrow), the internal

pterygoid muscle (dashed arrow)

and part of the parotid gland (thin

arrow). d Intraoperative view.

Extensive condylar involvement.

e Histology (haematoxylin-eosin


large atypical polygonal cells,

some with several nuclei (arrow)

Fig. 16 Stafne cyst discovered

incidentally. a OPT-like

reconstruction from CBCT data

set showing a well-defined,

unilocular radiolucency (arrow)

with sclerotic borders in the

region of 37 and 38. No

relationship to teeth. b Axial,c coronal and d 3D

reconstruction, posterior view.

Bony defect (arrows) in

characteristic location



15/17

material enhancement. Extension into the muscles of mastica-

tion is common, as well as loco-regional lymph node metasta-

ses. MRI essential to narrow the differential diagnosis, as OPT

and CT are non-specific. The presence of a destructive,

infiltrative pattern with enhancing nodules within the cyst wall,

as well as the presence of metastatic lymph nodes strongly

suggests a malignant tumour, thus making biopsy mandatory.

Primary intraosseous SCC

Primary intraosseous SCC is a very rare neoplasm resulting

from the malignant transformation of the epithelial lining of a residual cyst, follicular cyst or a keratocyst [13, 38]. In con-

sequence, as a general rule, following enucleation of any

cystic lesion in the mandible, a thorough examination of the

entire surgical specimen is mandatory to exclude the possibil-

ity of an intramural SCC that may have been overlooked pre-

operatively [39, 40]. Primary intraosseous SCC has a predi-

lection for men and typically occurs in the 6th – 8th decade.

There are less than 120 cases described in the literature. These

tumours are aggressive lesions with a high metastatic poten-

tial. Due to the non-specific clinical findings, most

intraosseous SCCs tend to be diagnosed at later stages.

Panoramic radiographs, CT and CBCT findings mimic benignfollicular cysts (Fig. 17) or radicular cysts. MRI and PET/CT

are the only modalities suggesting a malignant tumour.

Imaging findings on MRI are similar to those of intraosseous

mucoepidermoid carcinoma: solid tumour portions have low-

er signal on T2, whereas cystic portions display a high signal.

Enhancement of solid portions is typically seen after injection

of contrast material, as well as infiltration into the

perimandibular soft-tissues. ADC values of solid parts are

low, suggesting tumour components with high cellularity

(Fig. 17). On PET/CT, a high FDG uptake may be seen similar

to SCC arising from the mucosa of the upper aero-digestive

Fig. 17 Intracystic carcinoma. a Sagittal oblique and b axial CBCTimage

displaying the characteristic aspect of a dentigerous cyst with well-defined

cyst borders (arrows). The cyst surrounds the crown of an impacted tooth.

c T2-weighted image: solid intracystic component with moderately high

signal intensity (arrows). Fluid with high signal intensity within the cyst

(dashed arrow). Oedema in the masseter muscle (asterisk ). d ADC map

with low ADC values (circle) of solid parts (ADC = 0.89×10−3 mm2/s)

suggesting an intracystic malignant tumour despite the benign appearance

on CBCT. Histology revealed SCC arising within a dentigerous cyst

Fig. 18 Mandibular NHL.

a OPT. Difficulty to accurately

identify the lesion due its median

and paramedian position and the

typical anterior OPT artefact

(arrowheads) masking the lesion.

Subtle enlargement of the right

mental foramen (long arrow)

compared with the normal

contralateral side ( short arrow).

b , c T1-weighted unenhanced

axial images. d T1-weighted

fat-saturated contrast-enhanced

sagittal image. Large infiltrativelesion (asterisks ) extending from

the vestibule through the

mandible into the floor of the

mouth (arrows). The mandibular

cortical rim is mostly preserved

although the lesion shows diffuse

marrow infiltration



16/17

tract. Treatment consists of surgery with and without addition-

al radiotherapy.

Malignant lesions that may be missed on OPT

Mandibular lymphoma

Lymphomas are malignant tumours developed from cells of the lymphatic system and can therefore affect any organ

containing lymphoid tissue. While Hodgkin lymphomas

(HL) most often involve lymph nodes in the head and neck,

non-Hodgkin lymphomas (NHL) can equally affect extra-

nodal sites [41] such as the lacrimal glands, salivary glands,

muscles and soft tissues of the orbit, thyroid gland, maxilla

and mandible. Mandibular NHL is very rare. As it is frequent-

ly mistaken for dental infection, a prolonged delay in diagno-

sis can occur. All age groups can be affected, however adults

tend to be affected more often than children. There is no

gender predilection. The clinical features of mandibular

NHL are not specific and include pain, jaw swelling, ulcera-tion, tooth mobility and cervical lymphadenopathy. On pano-

ramic views, mandibular NHLs appear as ill-defined radiolu-

cent lesions. Despite their large size, the tumours can be easily

missed on conventional X-rays (Fig. 18). Radiological find-

ings can be quite subtle such as teeth displacement in the

occlusal direction and loss of the lamina dura with widening

of the periodontal ligament space [41]. Rarely, mandibular

NHL can present with minor osteolysis or with unilateral

enlargement of the mandibular canal and mental foramen

(Fig. 18). Enlargement of the mandibular canal and mental

foramen is rare and has been reported in neurogenic tumours

affecting the inferior alveolar nerve (schwannoma and neuro-

fibroma), in perineural spread of disease (mainly from SCC,

adenoid cystic carcinoma and lymphoma) and as an anatomic

variant mimicking pathology [42]. In our experience, in man-

dibular NHL, CT and MRI typically show minor or no

destruction of the cortical bone despite extensive infiltration

of the bony marrow and of the perimandibular soft tissues

(Fig. 18). As suggested in the literature, MRI provides

superior visualisation of submucosal tumour extension and

improved assessment of marrow infiltration compared with

CT or CBCT [43]. Low signal on T1 and T2, homogenous

contrast enhancement after injection of gadolinium chelates,

absent areas of necrosis despite the large size (Fig. 18) and low

ADC values (typically 0.6 – 0.8×10−3 mm2/s) are characte-

ristic findings. On PET/CT, mandibular NHL display high

FDG uptake and high SUV values (usually ≥10 – 15), similar

to lymphomas in other locations in the body. The differential

diagnosis of mandibular NHL includes other infiltrative

processes such as myeloma, leukaemia and bone metastases,

making biopsy mandatory for the correct histological

diagnosis. Treatment in mandibular NHL is done with

chemo(radio)therapy.

Conclusions

The vast majority of radiolucent lesions of the mandible seen

on conventional radiographs represent benign lesions that

require no further work-up. Nevertheless, certain radiological

features, such as large lesion size, bone scalloping, relation-

ship to an impacted tooth or the mandibular canal, tooth

resorption, as well as ill-defined lesion borders, require further radiological work-up. CT, CBCT, MRI and PET/CT are of

additional help if the nature of the lesion is unclear and for the

identification of those lesions, where biopsy is indicated for

definitive histology.

Open Access This article is distributed under the terms of the Creative

Commons Attribution License which permits any use, distribution, and

reproduction in any medium, provided the original author(s) and the

source are credited.

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http://dx.doi.org/10.1016/j.jcms.2012.11.002http://dx.doi.org/10.1136/bcr-2013-009102http://dx.doi.org/10.1055/s-0029-1214159http://dx.doi.org/10.1055/s-0029-1214159http://dx.doi.org/10.1007/s10006-012-0363-4http://dx.doi.org/10.1007/s10006-012-0363-4http://dx.doi.org/10.1111/j.1601-0825.2010.01781.xhttp://dx.doi.org/10.1111/j.1601-0825.2010.01781.xhttp://dx.doi.org/10.1007/s00405-012-2235-9http://dx.doi.org/10.1155/2011/387570http://dx.doi.org/10.1155/2011/387570http://dx.doi.org/10.1155/2011/387570http://dx.doi.org/10.1155/2011/387570http://dx.doi.org/10.1007/s00405-012-2235-9http://dx.doi.org/10.1111/j.1601-0825.2010.01781.xhttp://dx.doi.org/10.1111/j.1601-0825.2010.01781.xhttp://dx.doi.org/10.1007/s10006-012-0363-4http://dx.doi.org/10.1007/s10006-012-0363-4http://dx.doi.org/10.1055/s-0029-1214159http://dx.doi.org/10.1055/s-0029-1214159http://dx.doi.org/10.1136/bcr-2013-009102http://dx.doi.org/10.1016/j.jcms.2012.11.002

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